Abstract

Background Cannabis is commonly regarded as an innocuous drug and
the prevalence of lifetime and regular use has increased in most developed
countries. However, accumulative evidence highlights the risks of dependence
and other adverse effects, particularly among people with pre-existing
psychiatric disorders.

Aims To re-evaluate the adverse effects of cannabis in the general
population and among vulnerable individuals, including those with serious
psychiatric disorders.

Method A wide-ranging review of the topics related to these
issues.

Results and conclusions An appreciable proportion of cannabis users
report short-lived adverse effects, including psychotic states following heavy
consumption, and regular users are at risk of dependence. People with major
mental illnesses such as schizophrenia are especially vulnerable in that
cannabis generally provokes relapse and aggravates existing symptoms. Health
workers need to recognise, and respond to, the adverse effects of cannabis on
mental health.

UNTOWARD MENTAL EFFECTS OF CANNABIS

The untoward mental effects of cannabis may be classified:

Psychological responses such as panic, anxiety, depression or psychosis.
These effects may be described as ‘toxic’ in that they generally
relate to excess consumption of the drug.

Effects of cannabis on pre-existing mental illness and cannabis as a
risk-factor for mental illness.

Dependency or withdrawal effects.

The effects of cannabis on cognition are separately reviewed by Ashton
(2001, this issue).

PSYCHOLOGICAL RESPONSES TO CANNABIS

There is good evidence that taking cannabis leads to acute adverse mental
effects in a high proportion of regular users. Many of these effects are
dose-related, but adverse symptoms may be aggravated by constitutional factors
including youthfulness, personality attributes and vulnerability to serious
mental illness.

Cannabis and mood change

The acute response to cannabis generally includes euphoria and feelings of
detachment and relaxation. Adverse effects are not uncommon: these are
generally short-lived, but may persist or recur with continued use of the
drug.

From New Zealand, a sample of 1000 people aged 18-25 were asked to complete
a self-administered questionnaire on cannabis use and related problems
(Thomas, 1996). Those
respondents who admitted using cannabis (38%) were asked about mental health
consequences; of these, 22% reported panic attacks or anxiety. Women were
twice as likely as men to report these symptoms. Troisi et al
(1998) used urine tests on
Italian draftees to identify 133 men who used only cannabis. All individuals
with a pre-existing psychosis or severe personality disorder had been
excluded. An adjustment disorder with depressed mood was found in 16%, major
depression in 14%, and dysthymia in 10.5%. The severity of these symptoms was
dose-related. No acute psychotic symptoms were reported. Reilly et al
(1998) describe the adverse
effects found among 268 cannabis users who had taken the drug for at least 10
years, and who continued to smoke about two refers a day. The most common
adverse effects were feelings of anxiety, paranoia or depression (21%),
tiredness and low motivation (21%).

Among individuals making serious attempts at suicide, 16.2% met criteria
for cannabis misuse/dependence compared with 1.9% of controls — much of
the highly significant association was thought to be due to independent
variables including comorbidity, but it is suggested that cannabis misuse
makes a direct contribution to the risk of serious self-harm, either directly
or by aggravation of other mental disorders
(Beautrais et al,
1999).

Cannabis and psychosis

Cannabis use can lead to a range of short-lived symptoms such as
depersonalisation, derealisation, a feeling of loss of control, fear of dying,
irrational panic and paranoid ideas
(Thomas, 1993). For example,
Thomas (1996) reported that,
among cannabis users who responded to his survey, 15% identified psychotic
symptoms such as hearing voices or having unwarranted feelings of persecution
or risk of harm from others. Two small case studies have reported prolonged
depersonalisation after cessation of cannabis use
(Szymanski, 1981;
Keshaven & Lishman, 1986). ‘
Flashbacks’ or the subsequent partial re-experience when
drug-free of symptoms experienced during intoxication are rarely reported
after cannabis use (Thomas,
1993).

The casual use of the term ‘cannabis psychosis’ in clinical
psychiatric practice and in the scientific literature results in diagnostic
imprecision and research of uncertain validity. Thornicroft
(1990) reviews the possible
associations between cannabis use and psychosis and suggests that common
methodological failings are: (a) studies fail to adequately separate organic
from functional psychotic reactions to cannabis; (b) they have insufficiently
discriminated between psychotic symptoms and syndromes of a psychosis; and (c)
they have not balanced the weight of evidence for and against the category of
cannabis psychosis. Although there is good evidence for believing that
cannabis use may in certain circumstances contribute to psychotic disorders,
the connections are complex.

Hall et al (1994)
suggest that the fundamental questions are: is there a cannabis psychosis, and
does cannabis precipitate an underlying psychosis? In theory, cannabis use may
precipitate a psychosis in the following ways.

Acute use of large doses of the drug may induce a toxic or organic
psychosis with symptoms of confusion and hallucination, which remit on
abstinence.

Cannabis use may lead to an acute functional psychosis, similar to an acute
schizophreniform state and lacking the organic features of a toxic
psychosis.

Cannabis use may lead to a chronic psychosis, which persists after
abstinence.

Long-term cannabis use may lead to an organic psychosis which only
partially remits after abstinence, leaving a residual deficit state, sometimes
called an amotivational syndrome, which is thought to be analogous to the
chronic organic brain syndrome seen after prolonged misuse of alcohol.

Cannabis use may be a risk-factor for serious mental illness such as
schizophrenia.

Cannabis and toxic psychosis

Apart from single-case reports, the nature of cannabis-induced toxic
psychosis is considered in the following studies, all of which are weakened by
the lack of urine-testing to confirm the presence of cannabis and the absence
of other drugs of misuse.

Talbott & Teague (1969)
described 12 soldiers in Vietnam who, after their first admitted use of
cannabis, showed dis-orientation, impaired memory, confusion, reduced
attention span and disordered thinking with labile effect and hallucinations.
These symptoms resolved within a week. Tennant & Groesbeck
(1972) describe psychoses
among 36 000 US servicemen stationed in Germany. Of the 5120 soldiers using
cannabis at least three times a week, 720 presented with cannabis-related
problems. The hashish available was potent, containing 5-10%
tetrahydrocannabinol (THC). The authors identified 19 cases of a panic attack
or short-lived toxic psychosis, which appeared after a single high dose of
hashish, and a further 85 cases of toxic psychosis which appeared after the
consumption of cannabis with other drugs. These acute states tended to resolve
within 3 days.

From Calcutta, Chopra & Smith
(1974) retrospectively
identified 200 in-patients who showed serious psychiatric symptoms after
taking cannabis. The most common symptoms in all patients were sudden onset of
confusion, often associated with hallucinations and emotional lability.
Disorientation, depersonalisation and paranoid symptoms were common. Many
patients had taken a large dose of cannabis, which was followed by an
intoxicated state for which they were subsequently amnesic. Among the 34% of
patients without a previous history of psychiatric disorder, adverse symptoms
lasted no more than a few days, followed by full recovery. A previous history
of schizophrenia or personality disorder was associated with longer duration
of adverse symptoms.

From Pakistan, Chaudry et al
(1991) report on effects of
bhang, a potent beverage made from an infusion of cannabis leaves and
flowering tops. They identified 15 patients who having taken bhang,
presented with a psychosis with symptoms of grandiosity, excitement,
hostility, dis-orientation, hallucinations and thought disorder. Mental state
was assessed systematically, using the Brief Psychiatric Rating Scale (BPRS)
(Lukoff et al, 1986).
The control group of 10 patients all used bhang, but less frequently
than the study group.

This work suggests that cannabis, especially in high doses, can produce a
toxic psychosis in individuals who have no history of severe mental illness.
The main features are mild impairment of consciousness, distorted sense of
passage of time, dream-like euphoria, progressing to fragmented thought
processes and hallucinations, generally resolving within a week of abstinence
(Lishman, 1998).

Cannabis and acute functional psychosis

A number of studies suggest that heavy cannabis use can lead to an acute
functional illness, that is a state resembling the psychosis of acute
schizophrenia without the amnesia and confusion of a toxic psychosis.

Tennant & Groesbeck
(1972) identified 115 cases of
schizophrenic reaction among the 720 regular users of cannabis; however, all
but three had used cannabis with other drugs or alcohol. Thacore & Shukla
(1976) compared 25 individuals
with a putative diagnosis of ‘cannabis psychosis of the paranoid
type’ with controls diagnosed with paranoid schizophrenia. Patients with
cannabis psychosis showed more bizarre behaviour, violence, panicky affect,
more insight and less evidence of thought disorder. They also showed a rapid
response to neuroleptics with complete recovery. More robust in methodology is
the work of Rottanburg et al
(1982) in which 20 patients
with psychosis and with high urinary cannabinoids were compared with 20
matched cannabis-free controls. Mental state was assessed using the Present
State Examination (PSE) (Wing et
al, 1974). The cannabis-positive patients had more symptoms
of hypomania and agitation, less auditory hallucinations, flattening of
affect, incoherent speech and hysteria than controls. Clouding of
consciousness was absent in most cannabis patients. They also showed marked
improvements in symptoms within a week, while the controls remained unwell
despite receiving comparable antipsychotic drugs. The authors conclude that a
high intake of cannabis may be related to a rapidly resolving psychosis with
marked hypomanic features. However, 16 cannabis-positive psychotic patients
left the study prematurely, which may bias the findings on the 20 who
remained. Rapid resolution of symptoms is also reported by Carney et
al (1984), who identified
nine patients with cannabis-related psychotic episodes. Their differing
symptomatology was described as ‘schizophreniform, manic, delusional
psychosis and confusion’.

More recently, Mathers & Ghodse
(1992) carried out a
prospective study of in-patients with psychotic symptoms and cannabis-positive
urine. Blind to the urine test result, researchers applied the PSE on
admission and again at 1 and 6 months. Concurrently admitted patients with
psychosis but with drug-free urine analysis were controls. At 1 week the two
groups differed significantly on only five PSE items: changed perception,
thought insertion, non-verbal auditory hallucinations, delusions of control,
and delusions of grandiose ability; this symptom cluster at 1 week was thought
to be consistent with acute cannabis intoxication. These differences were
minor at 1 month and absent at 6 months. Chronic cannabis-induced psychosis
was not found. Caucasian patients were more likely to be depressed with
depersonalisation and derealisation, while African-Caribbeans showed more
culturally influenced delusions. However, these findings could not be
replicated by McGuire et al
(1994) who also used the PSE
to assess the psychopathology of 23 patients with psychosis who were
cannabis-positive on urinary screening, and 46 matched drug-free controls.
Cases and controls were indistinguishable in terms of psychopathology, DSM-III
diagnoses (American Psychiatric
Association, 1980), onset of recent illness, the proportion of
first admissions, ethnicity and socio-economic class, differing only in their
histories of substance use.

Having compared groups of drug-misusing patients with psychosis of varying
duration, Tsuang et al
(1982) concluded that the
shorter-duration disorders were drug-induced toxic psychoses, and the
longer-lasting disorders represented the expression of functional psychiatric
illness in vulnerable individuals. If corroborated, this suggests that the ‘
functional psychosis’ related to cannabis use is best explained
as a precipitated episode of an underlying functional illness.

Cannabis and chronic psychosis

Ghodse (1986) has suggested
that regular heavy users of cannabis may suffer repeated short episodes of
psychosis and effectively ‘maintain’ themselves in a chronic
psychotic state. This is a possibility, but Hall et al
(1994) note that it is
difficult to distinguish between a chronic cannabis psychosis and the
co-occurrence of an illness such as schizophrenia with continued cannabis use.
There is however, no robust evidence that heavy cannabis use may lead to a
psychotic illness which persists after abstinence
(Thomas, 1993).

Cannabis and amotivational syndrome

It has been suggested that heavy cannabis use could lead to an ‘
amotivational syndrome’ described as personality deterioration
with loss of energy and drive to work
(Tennant & Groesbeck,
1972). The supporting evidence largely comprises uncontrolled
studies of long-term cannabis users in various cultures
(Hall et al, 1994).
It is probable that amotivational syndrome represents nothing more than
ongoing intoxication in frequent users of the drug
(Negrete et al, 1986)
and the validity of this diagnosis remains uncertain
(Hall et al,
1994).

Cannabis as risk-factor for serious mentall illness

Comorbidity rates

Cannabis use is associated with high rates of comorbidity for other
psychiatric diagnoses. The Epidemiologic Catchment Area (ECA) survey
(Regier et al, 1990)
of 20 000 subjects in community and institutional settings showed that 50.1%
of individuals with cannabis dependence/misuse also met DSM-III criteria for
one other non-drug or alcohol mental disorder. Among 133 Italian draftees,
Troisi et al (1998)
found that the prevalence of comorbidity was significantly related to the
pattern of cannabis use: 69% of subjects with DSM-III-R cannabis dependence,
41% of those with cannabis abuse and 24% of occasional users reported at least
one DSM-III-R Axis 1 psychiatric diagnosis. Most common were adjustment
disorder with depressed mood (n=21), major depression (n=19)
and dysthymia (n=14). The severity of symptoms also increased with
degree of cannabis use. Psychotic symptoms were not found, but it should be
noted all individuals with psychotic illness or severe personality disorder
were not drafted.

There are high rates of drug misuse among people with mental illness. The
ECA study (Regier et al,
1990) showed that the risk of meeting criteria for a substance
misuse disorder was 4.6 times higher in those suffering from schizophrenia
than in the general population. Schizophrenia was associated with a six-fold
increase in risk of developing a drug use disorder, and cannabis was the most
commonly misused drug. Menezes et al
(1996) examined the prevalence
of substance misuse problems among 171 patients with psychotic illness who had
any contact with mental health treatment services in a south London area.
Alcohol problems were more prevalent, but current use of one or more drugs was
found in 35 subjects (20%); all but two said they used cannabis. Cantwell
et al (1999) studied
168 subjects presenting with a first episode of psychosis and found 1-year
prevalence rates of 19.5% for drug misuse, 11.7% for alcohol misuse, and
cannabis was the most commonly misused substance. Given these findings, it is
necessary to review the possible role of cannabis as a risk factor for
functional illness and for the aggravation of symptoms.

Effects of cannabis on severe mental illness

Given that high doses of cannabis can cause a toxic psychosis, then it may
be supposed it will aggravate the symptoms of schizophrenia. However, clinical
experience suggests that some patients say that they take cannabis as a form
of ‘self-medication’. For example, Dixon et al
(1990) interviewed 83 patients
with schizophrenia or schizophreniform psychoses who reported that cannabis
reduced anxiety and depression, led to increased suspiciousness and had varied
effects on drive and hallucinations. Arndt et al
(1992) investigated a cohort of
131 patients with schizophrenia and found that previous use of cannabis had no
impact on current symptoms. Peralta & Cuesta
(1992) reported that cannabis
had no significant effect on positive symptoms of schizophrenia, but it did
attenuate negative symptoms.

On the other hand, there are a few controlled studies that have tended to
demonstrate that cannabis aggravates the severity of positive symptoms.
Negrete et al (1986)
described the history of confirmed cannabis use in 137 patients with
schizophrenia in treatment. Subjects who were using cannabis over the 6-month
observation period presented with significantly greater delusions and
hallucinations, and made more use of psychiatric services. Similarly, Cleghorn
et al (1991) found
that drug-users with schizophrenia, among whom cannabis was the most heavily
used drug, had a higher prevalence of hallucinations, delusions and other
positive symptoms. This finding was replicated by Baigent et al
(1995), who reported that among
53 in-patients with a dual diagnosis of substance misuse and schizophrenia,
cannabis was the only drug that worsened positive symptoms.

Data from the ECA survey (Swanson
et al, 1990) also casts some light on the possible
effects of cannabis use disorder and violence. Subjects were asked about
episodes of violence in the previous year (i.e. hitting a partner, bruising a
child, fighting, using a weapon in a fight while drinking). Of the 191
respondents with cannabis abuse or dependence, 19.25% (risk ratio 9.4) had
been violent compared with 12.69% (risk ratio 6.2) of those with schizophrenia
or schizophreniform disorder and 24.57% (risk ratio 11.9) of those with
alcohol abuse or dependence. Here, the risk is expressed relative to the 2.05%
who were violent among those of the sample population who showed no
psychiatric disorder. However, this does not amount to a causal correlation
between cannabis co-morbidity and violence, given the possible role of
intervening variables such as individual and social factors.

That cannabis consumption also has an adverse effect on the course of
schizophrenia was noted by Negrete et al
(1986) and confirmed in a
prospective study by Linszman et al
(1994). A cohort of newly
admitted patients with schizophrenia were assessed monthly for a year, using
the BPRS and self-reports of cannabis use. The cannabis-using group
(n=24) experienced significantly more and earlier psychotic relapses
and this effect was dose-related.

As Hall et al
(1994) remark, these findings
are a slender basis on which to draw conclusions about the effect of cannabis
on schizophrenic symptoms. Until further prospective studies have been carried
out, it would be prudent to regard cannabis as a vulnerability factor in
relation to major mental illness and to caution at-risk individuals against
using the drug.

Cannabis as risk factor for mental illness

There is no evidence that cannabis is a causal factor in schizophrenia and
it is more relevant to consider whether the misuse of the drug constitutes a
risk factor for this illness. Supporting evidence is found in a prospective
study by Andreasson et al
(1987) of 45 570 Swedish
conscripts, of whom 9.4% had used cannabis and 1.7% were ‘high
consumers’ having used more than 50 times. Fifteen-year follow-up data
were drawn from national registers of deaths and psychiatric cases. Compared
with non-users, the relative risk of schizophrenia was 2.4 in the group that
reported use of cannabis at least once, rising to 6.0 among heavy users.
Nearly half (430/730) of these high consumers had a psychiatric diagnosis
other than psychosis on conscription; controlling for this reduced the
relative risk to 2.9. The authors suggest that cannabis consumption is a ‘
life-event stressor’ for individuals vulnerable to schizophrenia.
Hall et al (1994)
offer a number of alternative explanations. There is a large temporal gap
between self-reported cannabis use on conscription and the development of
schizophrenia over 15 years, and no data as to whether the cannabis use
continued during this time. Drugs other than cannabis could have been taken at
any time after conscription.

It should also be noted that as only 49 of the 274 conscripts with
schizophrenia had ever tried cannabis, then this drug may only be relevant to
a minority of cases. Furthermore, Jablensky et al
(1992) demonstrate a striking
uniformity in the incidence of schizophrenia in cultures with very different
rates of cannabis consumption.

The possibility of a genetic explanation for the association between
cannabis use and schizophrenia was raised by McGuire et al
(1994). In this study, 23
patients with psychosis and with cannabis in their urine were gender-matched
with 46 drug-free controls with psychosis, and the lifetime risk of
psychiatric disorder among all the first-degree relatives was ascertained. The
cannabis-positive subjects had a significantly greater (7.1%) familial risk of
schizophrenia than controls (0.7%), suggesting that the development or
recurrence of acute psychosis in the context of cannabis use may be associated
with a genetic predisposition to schizophrenia.

CANNABIS DEPENDENCE

Evidence for cannabis dependence

It had been believed that cannabis use did not lead to tolerance and that
there was no withdrawal syndrome. However, since the mid-1970s, these views
have been challenged by many experimental and observational studies. For
example, Jones & Benowitz
(1976) administered oral THC
in doses of 70-210 mg/day to subjects for 30 days and noted a progressive loss
of the subjective ‘high’. This finding was replicated by Georgotas & Zeidenberg (1979), who
gave an average daily dose of 210 mg THC to volunteers for a 4-week period —
the subjects then “found that the marijuana was much
weaker”. Withdrawal signs were also found: during the first week of
abstinence the subjects “became very irritable, uncooperative, resistant
and at times hostile”; they also became hungry and experienced insomnia.
These effects waned over 3 weeks. Cessation of smoked cannabis has also been
shown to lead to withdrawal symptoms
(Haney et al, 1999).
The cannabis-withdrawal syndrome has now been unequivocally demonstrated and
includes restlessness, anxiety, dysphoria, irritability, insomnia, anorexia,
muscle tremor, increased reflexes and autonomic effects including changes in
heart rate, blood pressure, sweating and diarrhoea. The syndrome may appear in
about 10 hours, and peaks at about 48 hours
(Mendelson et al,
1984).

The validity of cannabis dependence

The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV;
American Psychiatric Association,
1994) presents criteria for the diagnosis of psychoactive
substance dependence, based largely on the concept of the dependence syndrome
(Edwards et al,
1981). The key features of DSM-IV substance dependence are
cognitive, behavioural and physiological symptoms, indicating that the
individual continues to use the substance despite significant
substance-related problems. The criteria include tolerance, a withdrawal
syndrome, difficulty in controlling consumption and a pattern of use which
leads to a reduction in other important activities. In an empirical study,
Morgenstern et al
(1994) found the DSM concept
of cannabis dependence as least as valid as those for dependence on alcohol,
opiates, stimulants and sedatives.

Prevalence and course of cannabis dependence

From ECA data, Anthony & Helzer
(1991) showed that men had a
higher prevalence (7.7%) of cannabis abuse or dependence than women (4.8%).
This was largely due to the greater exposure to illicit drugs of men, since
the prevalence of a diagnosis of abuse/dependence among those who had used
cannabis more than five times was the same in men and women (21% and 19%,
respectively). Extrapolating from these data, Hall et al
(1994) suggest that about 17%
of those who used cannabis more than five times would meet DSM-III criteria
for dependence, and that for those who have ever used there is approximately a
1/10 risk.

From a New Zealand birth cohort of 1265 children, Fergusson & Horwood
(2000) found that by the age
of 21, nearly 70% had used cannabis and over 9% met DSM-IV criteria for
cannabis dependence. Key predictors were male gender, ethnic minority status
and measures of adolescent risk-taking behaviours, including cigarette
smoking, conduct problems and a delinquent peer group.

Wiesbeck et al
(1996) set out to determine
the prevalence of the cannabis-withdrawal syndrome in people who had used the
drug but who were not in treatment. In a cohort of 5611 individuals, 31% had
taken the drug on more than 21 occasions in a year. Among these more frequent
users, 16% met criteria for a cannabis-withdrawal syndrome — i.e. at
least any one of the following: feeling nervous or irritable, insomnia,
tremor, sweats, nausea, gastrointestinal disturbance or appetite change. These
individuals had used the drug almost daily for an average of 70 months and
even when use of alcohol and other drugs was considered, cannabis use was
still significantly related to a self-report of a history of cannabis
withdrawal.

Thomas (1996) found that
35% of cannabis users said that they could not stop when they wanted to, 24%
continued to use despite problems attributed to the drug and 13% felt that
they could not control their consumption. Restlessness or irritability if they
could not use cannabis was reported by 20% of those surveyed. Interestingly,
dependent users were no more likely to report panic or psychotic episodes than
those classed as non-dependent. With regard to untoward social consequences,
14% of cannabis users agreed that the consumption of the drug had caused them
to neglect activities previously considered important or enjoyable. These
findings (Thomas, 1996) have
to be qualified by the low overall response rate of 35%, the use of
unvalidated criteria for cannabis dependence and by the lack of data on misuse
of alcohol or other drugs among the sample.

Swift et al (1998)
interviewed a sample from New South Wales of 243 long-term cannabis users who
were smoking 3-4 times a week. A lifetime prevalence of 57% was found for both
DSM-III-R and ICD-10 (World Health
Organization, 1992) dependence, but only a quarter perceived that
they had a cannabis problem.

VULNERABILITY TO ADVERSE EFFECTS OF CANNABIS

It has previously been emphasised that constitutional factors such as
relative youthfulness, personality and misuse of other drugs, may act as
vulnerability factors to the adverse mental effects of cannabis. Mental
illness as a vulnerability factor has been reviewed in the previous
section.

Adolescence

There are a number of reasons why adolescence may be regarded as a time of
vulnerability for the adverse mental effects of cannabis. First, adolescents
may experience emotional problems that cue cannabis use, and their relative
youth may lead to an increased risk of adverse mental states on using the
drug. Second, regular use of cannabis may interfere with learning and personal
development. Last, early initiation of cannabis use may predict an increased
risk of escalation in risk and progression to other drugs.

With regard to the possible impact of emotional problems, Newcombe &
Bentler (1988) found a strong
relationship between adolescent drug use and the experience of emotional
distress, depression and lack of a sense of purpose in life. As to the
prospect of adverse mental states on using high doses of cannabis, this review
has demonstrated dose-related effects in adults and the younger user is not
likely to be at any lesser risk. Crowley et al
(1998) found that for
adolescents with conduct problems, cannabis use was not benign in that misuse
was associated with high rates of dependence and withdrawal.

The possible effects of cannabis consumption on the educational performance
of adolescents are not easy to demonstrate in population studies
(Hall et al, 1994).
Newcombe & Bentler (1988),
having controlled for the higher nonconformity and the lower academic
potential among adolescent drug users, found only a modest negative link
between drug use and college involvement. Schwartz et al
(1989) found short-term memory
impairment in 10 cannabis-dependent adolescents compared with matched
controls. Test results tended to improve over 6 weeks, which suggested that
the deficits observed were due to past cannabis use.

Polydrug use

A substantial number of young people in the community use a range of drugs
which includes cannabis. Ramsay & Percy
(1996) found that 4% of a
group of 16- to 29-year-olds admitted using cannabis and other drugs in the
past month, by contrast with 8% who had used only cannabis. Clinical
observation suggests that cannabis users who also misuse other drugs or
alcohol seem to experience more severe mental health problems than those who
solely take cannabis, but there do not appear to be any substantial published
studies on this issue. Polydrug use is a recognised concern in psychiatric
populations: for example, Baigent et al
(1995) found that 20% of their
dual-diagnosis #patients misused more than one substance.

Personality

Given the heterogeneity of the population of cannabis users, it is not
surprising that no single personality type or disorder is particular to users
of that drug or, indeed, to users of any illicit drug
(Allen & Frances, 1986).
However, it is a matter of clinical observation that the use of cannabis by
some individuals seems to be predisposed by traits such as social anxiety,
anxiety or dysphoria. Such posited use as a form of self-medication to relieve
unwanted affects or feelings was not corroborated in a study of
cannabis-dependent individuals (Greene
et al, 1993). There is good evidence for the comorbidity
of drug misuse and some personality disorders. For example, Regier et
al (1990) report that
some form of substance abuse was identified in 83.6% of individuals with
antisocial personality disorder (ASPD), with an odds ratio of 29.6. It should
be appreciated that this very high rate arises because substance abuse is one
of the major diagnostic criteria for ASPD; only 16% of individuals with ASPD
did not have a history of substance abuse. The same study showed that the
lifetime prevalence of ASPD in cannabis abuse or dependence was 14.7% with an
odds ratio of 8.3. The interaction between ASPD and cannabis use is too
complex to explore at length in this review, but it is probable that each
disorder exacerbates the adverse effects of the other. See Dolan & Coid
(1993) for a discussion of
factors determining outcome in ASPD.

Implications for mental health care

How should mental health services respond to these findings? The key
priorities are: (a) risk-management and care-planning have to be informed by a
thorough substance-misuse assessment
(Johns, 1997); (b) community
and in-patient psychiatric services should develop policies on substance use
which balance the treatment needs of individual patients with duties of care
to other patients and to the general public; and (c) research is needed into
treatment interventions for patients with mental illness and substance misuse
problems.

Clinical Implications and Limitations

CLINICAL IMPLICATIONS

Among those who have ever taken cannabis, 1/10 are at risk of
dependence.

Heavy cannabis misuse leads to the risk of psychotic episodes, and
aggravates the symptoms and course of schizophrenia.

For any psychiatric patient, risk-management and care-planning is
incomplete without a thorough assessment of substance misuse.

LIMITATIONS

The available literature shows a preponderance of case reports and
uncontrolled studies.

Epidemiological findings from one setting cannot be assumed to
generalise to other cultural groups.

It is not easy to determine causal explanations from the studies
cited.